High concentrations of metal ions such as copper and iron in the brain have been considered as an essential factor for the covalent crosslinking of Aβ, and thus an important trigger of the onset of amyloidosis pathology in Alzheimer's Disease (AD). Structurally, two imidazoliums of H13 and H14 of an Aβ peptide serve as essential binding sites for metal coordination. This coordination could bring two or more Aβ peptides into close proximity for initialization of irreversible Aβ crosslinking. Metal ion chelators have been tested for AD treatment with the purpose of retardation of Aβ aggregation. However, one of the obvious and potential side effects of the metal chelators is the disruption of brain metal homeostasis during prolonged treatment. Structurally, all of the reported chealtors are bi- or tri-dentate ligands for metal ions; therefore a single molecule could coordinate with a metal ion to form an intramolecular complex (FIG. 1a). Before reaching the target (or targeting region), they could sequester/seize metal ions that may be essential for normal brain functions.